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Biology of Sport, Vol. 22 No2, 2005
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EFFECT OF ANABOLIC-ANDROGENIC STEROIDS ON THE ACTIVITY
OF RENNIN-ANGIOTENSIN-ALDOSTERONE SYSTEM,
ECHOCARDIOGRAPHY PARAMETERS AND ON THE BODY MASS IN
BODY BUILDERS
K.Chrostowski1, M.Szczypaczewska2, K.Anioł-Strzyżewska3, D.Kwiatkowska1,
R.Grucza1
1
Dept. of Antidoping Research, 2Outpatient Clinic, 3Dept. of Biochemistry, Institute
of Sport, Warsaw, Poland
Abstract. This study was performed in groups of body builders: Group I (18
subjects) in whose metabolites of anabolic-androgenic-steroids (AAS) were
detected in urine, and Group II (22 subjects) where no AAS were found in urine.
Echocardiography parameters, aldosterone, rennin activity in plasma and AAS
metabolites in urine were measured. The results of both groups of body builders
were compared with those obtained in 30 cyclists and 26 rowers (no AAS detected).
It was found that plasma aldosterone level in body builders correlated well with the
heart echocardiography parameters, body mass index (BMI) and with the activity of
serum angiotensin converting enzyme (ACE). No such relationship existed in tested
rowers and cyclists. These groups were characterised by statistically significant
relation between aldosterone level in blood plasma and the rennin plasma activity
(ARO) which, on the other hand, was not found in the groups of body builders. The
correlation between aldosterone level and the rennin blood plasma activity in
cyclists and rowers might be an effect of strong stimulation of RAAS (higher in
cyclists than rowers) resulting from the intense physical effort. Lack of such
relation in body builders might be caused by a stronger tissue activation of the
RAAS modifying aldosterone activity and bringing in result an increase in body
mass and left ventricle hypertrophy. Results of the study suggest, therefore, that
supra-physiological doses of AAS could enhance tissue activity of the renninangiotensin-aldosterone system (RAAS) what, with coincidence, of other
pathogenic factors (i.e.: inflammatory states, toxic substances, injuries, great stress)
may play an important role in the process of pathogenesis of the cardiovascular
disorders leading to a sudden heart attacks.
(Biol.Sport 22:191-205, 2005)
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Reprint request to: Dr Maria Szczypaczewska, Outpatient Clinic, Institute of Sport, Trylogii
2/16, 01-982 Warsaw, Poland; E-mail: [email protected]
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Biol.Sport 22(2), 2005
Key words: Doping – Steroids – Echocardiography – Angiotensin – Aldosterone –
Body builders
Introduction
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Several clinical trials showed that application of anabolic-androgenic steroids
(AAS) in the normal, pharmacological doses has an advantageous effect in many
diseases and is completely safe during therapy [16]. On the other hand, the longlasting non medical intake of large doses of steroids (described as a supraphysiological or mega doses) by men and women attending fitness clubs can
seriously harm their health [3,8,19,22,26,28,32,34]. Although effects of application
of the supra-physiological doses of AAS by athletes, for the purpose of muscle mass
growth and better results in force disciplines of sport were confirmed in recent years
[1] but the physiological mechanism of this phenomenon remains unclear. A long
term of AAS intake may bring various side effects resulting in serious health
damages [3,12,13,22,24,28]. Overdoses of AAS causes cardiovascular disorders
such as hypertrophy of the left ventricle of the heart, arterial hypertension, cardiac
arrhythmia, blood clotting, coronary blood flow disability, myocardium
inflammation, acute coronary inefficiency, cardiac infractions, arterial sclerosis,
circulatory failure and heart attacks which may end of sudden death in people
willing to achieve a sport success by any costs [8,12,17,18,19,34]. Overdoses of
AAS can also trigger some mental instability in the form of a maniac-depressive
states expressed by uncontrolled aggression or deep depression associated with
some suicidal inclinations [10,18,24,26,34].
On the other hand, despite of the mass application of AAS by youngsters and
adults, only relatively small number of the mentioned health disorders was noted,
especially under controlled circumstances [1]. As a consequence, there are some
opinions in medical society that those casuistic cases might be exaggerated when
side effects (cardiovascular in particular) of large doses of AAS are considered
[8,13,29,32,33].
In pathogenesis of cardiovascular diseases (especially of the left ventricle
hypertrophy, vascular disturbances and cardiac infractions) some attention was
focused on the role of rennin-angiotensin-aldosterone system (RAAS), specifically
on its important effectors angiotensin II and aldosterone [6,7,9,23,31]. Beyond the
well known hormonal or circular activity of the above system regulating the arterial
blood pressure and water-electrolyte balance, the recent publication show that all
basic elements of RAAS are synthesized in many organs e.g.: heart muscle, skeletal
Effect of AAS on the activity of RAAS
193
Biol.Sport 22(2), 2005
muscles, vessels endothelium, brain, kidneys and reproductive organs
[5,20,30,31,36].
It should be noted that tissue synthesis of aldosterone is enhanced in overgrown
organs that is also in heart muscle and skeletal muscles [5,7,20,21,23,29,36]. The
organic or tissue RAAS exhibits a local activity intracellular, on cells sphere or
inside of the neighbouring cells. The system functions through the stimulation of the
cascade of tissue mediators and growth factors which can elicit a hypertrophy of in
skeletal muscles, heart muscle or vessels smooth muscles, or the reverse can cause
the muscles atrophy [23,31,36]. The tissue activity of the rennin-angiotensinaldosterone system is a crucial element in regulation of the cardiovascular system
under pathological conditions as well as during the adaptation process adjusting the
cardiovascular system to the intense physical efforts performed by athletes
[5,6,7,9,21,30,35].
Our previous study revealed an increased aldosterone level in blood plasma in
subjects currently using AAS and in those who recently ceased using the AAS [3].
The question therefore raised, whether the organism’s response to overdoses of
AAS elicit both, the “profitable” (skeletal muscles mass increase) and unfavourable
(causing morbid symptoms) effects by changed activity of the rennin-angiotensinaldosterone system (RAAS) [3].
The aim of this study was to investigate possible relationship between the left
ventricle hypertrophy of the heart, echocardiography parameters, body mass and
levels of plasma markers of RAAS activity in subjects using supra-physiological
doses of anabolic-androgenic steroids (body builders) and in sportsmen not using
AAS (cyclists and rowers).
Material and Methods
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The study was performed on 40 body builders, amateurs or former athletes.
Informed, written consent of the subjects was obtained and experiments were
accepted by the Ethics Committee of the Institute of Sport.
The body builders were divided into two sub-groups. The first, determined as
“positive” consisted of 18 subjects in whose anabolic-androgen steroid metabolites
were present in urine samples. The second group, “negative” included 22 subjects
whose urine samples did not contain any AAS metabolites.
Table 1 and Table 2 present basic characteristics of the subjects including age,
years of AAS application, number of cycles of the AAS application, weeks of AAS
intake in the last cycle, type and amount of recently used medicine and AAS
metabolites found in urine. Table 1 shows data of 9 body builders who declared
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K.Chrostowski et al.
Biol.Sport 22(2), 2005
current taking of AAS (“on cycle”) while Table 2 the data of 9 body builders in
whose AAS metabolites were detected in urine samples (mainly nandrolone) though
they claimed not taking the steroids at least in the period of 1-12 months.
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Table 1
Characteristic of body builders declaring current intake of SAA (”on cycle”)
No
Age
(years)
1
46
2
33
3
23
4
30
5
33
6
29
Years
Weeks Amount AAS metabolites
Doses of drugs
of AAS of intake of cycles detected in urine consumed during the last
applica- during
in life
cycle
tion
cycle
(mg)
17
6
51
Metenolone,
Metandienone, 610 mg,
Stanozolol,
Nandrolone, 600 mg,
T/Et* - 33.2
Testosterone, 7000 mg
3
12
7
19-NA**-547
Metandienone, 550 mg,
ng/ml
Nandrolone, 1500 mg
Metenolone I, II
Testosterone, 875 mg,
Clenbuterol, 720 mg
HCG, 24 u,
Insulin, 60 u
2
8
3
19-NA - 221
Metandienone, 1000 mg,
ng/ml
Nandrolone, 1800 mg,
Omnandren, 3500 mg,
Gonadotropin, 6000 u
11
4
4
19-NA - 227
Oxandrolone, 850 mg,
ng/ml
Boldenone, 800 mg,
Epimetendiol;
Vinstrol, 1600 mg
Stanozolol,
Oxandrolone,
T/Et - 76
5
8
6
Boldenone II,
Nandrolone, 2250 mg
Metenolone I,II
Omnandrene, 2000 mg
Clenbuterol, HCG
8
12
6
19-NA – 255.6 Metandienone, 1000 mg
ng/ml
Nandrolone, 1000 mg
Epimetendiol,
Omnandren, 3000 mg
3’stanazolol
Oxandrolone
T/Et – 75.6
195
Effect of AAS on the activity of RAAS
Biol.Sport 22(2), 2005
7
29
7
8
12
8
31
10
6
30
9
28
1,5
1
7
19-NA – 56.5
ng/ml
Metandienone, 1250 mg
Primabolan, 1200 mg
Testosterone, 1500 mg
Primobolan, 400 mg
Sustanon, 2000 mg
HGH, 84 u
Metenolone I, II;
T/Et - 41,
19-NA - 7 ng/ml
DHT***.
3’,4’Beta
Metandienone, 1505 mg,
Stanozolol
Vinstrol, 1000 mg
*T/ET - ratio of testosterone to epitestosterone; **19-NA - 19 norandrosterone;
***DHT=dihydrotestosterone
Table 2.
Characteristic of the body builders declaring not taking AAS during the time of
experiments (”off cycle”), though they urine samples still contained some steroid
metabolites
Age Years of Period in
Amount Amount
(years)
AAS
cessation of of weeks of cycles
applicaAAS
during the in life
tion
application
cycle
(months)
10 23
4
3
7
4
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No
11
23
2
3
7
3
12
20
3
1
5
5
13
24
3
3
8
4
14
19
3
1
12
1
AAS
metabolites
detected in
urine
Metenolone
I, II
Doses of drugs
consumed during the
last cycle
(mg)
Metandienone, 1050 mg
Oxandrolone, 612 mg
HCG, 6000 u
Metandienone, Metandienone, 1470 mg
19-NA, 43
Nandrolone, 350 mg
ng/ml
Testosterone, 9000 mg
19-NA, 325
Metandienone, 1500 mg
ng/ml
Nandrolone, 600 mg
Testosterone, 6500 mg
HCG, 1000 u
19-NA, 22
Nandrolone, 1000 mg
ng/ml
Vinstrol, 800 mg
19-NA, 18.5 Metandienone, 1000 mg
ng/ml
Nandrolone, 1250 mg
THC, 13.5
Testosterone, 2500 mg
ng/ml
Vinstrol, 500 mg
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Biol.Sport 22(2), 2005
15
29
7
2
6
7
19-NA, 56.5
ng/ml
16
34
10
1
8
6t
19-NA, 34.3
ng/ml
17
16
1
1
7
1
18
30
11
2,5
6
36
19-NA, 34.9
ng/ml
19-NA, 50
ng/ml,
3’OH
Stanozolol.
Metandienone, 1250 mg
Primabolan, 1200 mg
Testosterone, 1500 mg
Metandienone, 1500 mg
Nandrolone, 250 mg
Testosterone, 2000 mg
Metenolone, 750 mg
Metandienone, 1000 mg
Omnandren, 1750 mg
Oxandrolon,850 mg
Boldenon, 800 mg
Vinstrol, 1600 mg
Among 18 tested subjects, the nandrolone (19-nor-androsterone) concentration in
urine exceeding the level of 2ng/ml (for men) was found in 8 samples. Next 6
samples contained both nandrolone and other steroid metabolites. In last 4 samples
various anabolic steroid metabolites were found.
Results of the study performed in body builders were compared with data
attained from 30 road cyclists and 26 rowers. None of the above mentioned athletes
showed any presence of the AAS metabolites in urine nor the steroid profile
disturbances.
Each subject filled up the questionnaire concerning the AAS type and intake
history and observed health disorders. Next, the subject was medically checked
including ECG recordings (Marquette Hellige).
The echocardiography examination was conducted by the ACUSON apparatus.
The evaluation of measurements was made always by the same person. The left
ventricle mass (LVM) of heart was counted according to the formula of Devereux:
0.8[1.04(IVSd+LVdD+PWd)3-LVdD3]+0.6 g.
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Other indices were also calculated: LVM in transformation to subjects height in
cm taking the border value of >1.7 g/cm or 170 g/m [35]; heart mass index (g/m2)
describing the left ventricle mass to body surface area (MIM) taking the proper
border value up to 143 g/m2 [14]; left ventricle dimension of diastole (LVdD) (cm);
inter-ventricular septum diastole dimension (IVSd) (cm) and left ventricle posterior
wall dimension of diastole (PWd) accepting the border value of 1.2-1.3 cm [35].
Effect of AAS on the activity of RAAS
197
Biol.Sport 22(2), 2005
After 12 h fasting from each subject the blood sample from cubital vein was
taken into two separate tubes. The first tube, filled with a sodium versenate was
designated for aldosterone and rennin plasma activity (ARO) measurements. It was
whirled in chilled centrifuge and kept in 80 ْ C for further analyses. In the second
tube the blood for a clot for biochemical and hormonal analyses as well as for
determination of angiotensin converting enzyme (ACE) activity was collected.
All subjects were asked to collect a 24-hour urine sample, used for detection of
anabolic steroid metabolites and for the evaluation excretion of sodium and
potassium. Aldosterone level in plasma was estimated by the method of IgnatowskaŚwitalska adapted for the blood plasma assay [11]. The aldosterone in plasma was
extracted with dichloromethane and determined in duplicates with the RIA method
using the aldosterone antibodies of SIGMA #A3793, marked by tritium of
aldosterone (ELKABE-Amersham) and standard of aldosterone (Peninsula).
Applied antibodies showed lower than 0.001% cross reaction with the cortisone,
corticosterone and dezoxycorticosterone. The coefficients of the method variability
was 8% for intra-serial and 12% for inter-serial [11]. Plasma rennin activity was
determined with the RIA method (Immunotech kit Cat#3518). The angiotensin
converting enzyme (ACE) activity was measured according to the Liberman method
[15].
Statistical Analyses
The mean values (±standard deviation) of the results in respective groups were
calculated with the ANOVA test by STATISTICA StatSoft Programme v6. Because
of non-parametric distribution of the data the statistical significance of differences
were estimated with Kruskal-Willis tests for independent groups. The correlation
coefficients for intra groups were marked with the non-parametric rank test of
Spearman, accepting the significance level at p<0.05.
Results
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Table 3 presents the mean values (±SD) of results obtained in 40 body builders,
26 rowers and 30 cyclists. The statistical analysis showed a significant differences
regarding the anthropometrical parameters such as age, body mass, height, body
mass index (BMI) and body surface area (BSA). The group of body builders
differed from rowers and cyclists with age, body mass, BIM and BSA.
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Biol.Sport 22(2), 2005
Table 3
Biophysical characteristics of the subjects and echocardiography parameters of the
left ventricle of the heart, rennin plasma activity (ARO), angiotensine converting
enzyme (ACE) activity and levels of plasma aldosterone (ALDO) in groups of:
culturists, cyclists and rowers (ANOVA test: means ± SE)
Number of subjects
Age (years)
Body mass (kg)
Height (cm)
Body mass index
BMI (kg/ m2)
Body surface area
BSA (m2)
Left ventricle mass LK (g)
Left ventricle
mass/height (g/cm)
MIM (g/m2)
LVdD (cm)
IVSd (cm)
PWd (cm)
ARO u/ml/h
ACE (mU/ml)
ALDO (ng/dl)
ALDO/ARO
Systolic blood
pressure (mm Hg)
Diastolic blood
pressure (mmHg)
1. Body
builders
40
29.21.3
92.71.8
176.40.9
29.80.5
2. Rowers
3. Cyclists
Statistical
significance
1 vs 2 1 vs 3 2 vs 3
***
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***
***
***
**
**
NS
NS
***
**
NS
26
20.71.1
86.21.7
189.21.3
23.90.3
30
26.10.6
74.81.1
181.31.2
22.70.2
2.030.02
2.130.02
1.940.02
*
***
**
259.48.8
266.28.6
262.78.8
*
NS
NS
1.470.04
1.40.04
1.450.04
***
*
NS
122.73.2
125.13.4 135.24.3
5.480.06
5.570.05 5.490.06
1.150.012
1.550.02 1.170.02
1.1470.014 1.1460.015 1.1570.02
2.370.27
1.040.15
1.660.2
30.21.3
29.51.5
25.81.2
9.950.8
9.51.1
13.51.3
7.01.0
12.41.3
10.01.0
127.51.6
125.41.4 112.52.2
*
NS
**
*
***
*
***
NS
***
NS
NS
NS
NS
***
***
NS
NS
***
*
NS
NS
NS
**
NS
**
NS
**
***
***
NS
81.21.1
76.10.9
711.2
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Significance of average differences in groups evaluated with the test of KruskalWillis; p value for repeated comparisons;
*p<0.05; **p<0.01; ***p<0.001; NS - no significant
Abbreviations:
MIM – heart mass index (g/m2) = left ventricle mass / body scope area,
Effect of AAS on the activity of RAAS
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Biol.Sport 22(2), 2005
LVdD – diastolic dimension of the left ventricle,
IVSd – diastolic dimension of the ventricular septum,
PWD – diastolic dimension of the left ventricle posterior wall,
ARO – plasma renin activity
ACE – conversionary enzyme activity,
ALDO - aldosterone
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The left ventricle mass (g), heart muscle mass index (MIM) (g/m2), diastolic
dimension of the inter-ventricular septum (IVSd) (cm) were significantly greater in
rowers than in body builders. In contrast, the left ventricle mass/height index (g/cm)
and the dimension of the left ventricle posterior wall during diastole (PWd) (cm)
were greater in body builders than in rowers. No significant differences were found
in the echocardiography parameters between body builders and cyclists with the
exception of the left ventricle mass index (g/cm) which was statistically higher in
body builders. In the echocardiography parameters the only difference found
between rowers and cyclists was the MIM values (p<0.043). The diastolic
dimension of the left ventricle (LVdD) (cm) did not differ significantly in all tested
groups.
The rennin plasma activity (ARO) differed significantly between the groups of
subjects. The greatest values of ARO were found in body builders but the ARO was
lower in rowers than in cyclists (p<0.008). The ACE activity was significantly
greater in body builders than in cyclists (p<0.002) and rowers (p<0.0002). Mean
values of aldosterone level in plasma differed significantly between body builders
and rowers (p<0.0003).
The systolic (RRs) and diastolic (RRd) arterial blood pressures were clinically
accepted limits for all groups of subjects. However, the mean values of (RRs) were
significantly greater in the group of body builders comparing with rowers and
cyclists. Also the diastolic blood pressure (RRd) was greater in body builders.
Important differences between groups of subjects were found during the intragroup analyses regarding aldosterone in blood plasma, anthropometrical parameters
and the left ventricle of heart dimensions as well as of the rennin plasma activity.
The results of the analyses are presented in Table 4. In body builders some positive
correlation coefficients were found between aldosterone level and the following
echocardiography parameters: left ventricle mass, left ventricle mass index/height,
diastolic dimension of the left ventricle septum (IVSd) as well as the body mass
index (BMI), aldosterone level and ACE activity in the blood serum. Such
relationships were not found for rowers and cyclists. Instead, a significant
correlations were found for aldosterone levels in plasma and rennin plasma
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Biol.Sport 22(2), 2005
activities were found in rowers and cyclists. Alike correlations did not occur in the
group of body builders.
ECG did not revealed any significant deviations fro clinical norm in all groups of
subjects.
Table 4
Correlations of rank order, according to Spearman, between levels of aldosterone in
blood plasma (ALDO) and anthropomorphic data, echocardiography parameters of
the left ventricle of heart, ARO and ACE activities and systolic and diastolic blood
pressures (ANOVA test)
Tested groups
Number of subjects
Aldosterone in plasma (ng/dl)
Body mass (kg)
Body builders
Rowers
Cyclists
40
26
30
ALDO
ALDO
ALDO
0.307 *
Height (cm)
-0.07 (NS) -0.018 (NS)
0.014 (NS)
0.08 (NS)
-0.07 (NS)
0.317 *
-0.15 (NS)
0.05 (NS)
0.27 (NS)
-0.04 (NS)
0.18 (NS)
0.33 *
-0.19 (NS)
0.14 (NS)
0.33 *
-0.17 (NS)
0.13 (NS)
0.22 (NS)
-0.05 (NS)
0.03 (NS)
LVdD (cm)
0.31 *
-0.21 (NS)
0.26 (NS)
IVSd (cm)
0.33 * 0.009 (NS) -0.0004 (NS)
2
Body mass index BMI (kg/m )
2
Body surface area BSA (m )
-1
Left ventricle mass (g.m )
-1
Left ventricle mass/height (g.m /cm)
-1
2
MIM (g.m /m )
PWd (cm)
0.25 (NS)
0.07 (NS)
0.12 (NS)
ARO (ng/ml/h)
0.17 (NS)
0.55 **
0.68
0.32 *
0.09 (NS)
-0.11 (NS)
0.29 (NS)
0.11 (NS)
0.07 (NS)
Systolic blood pressure RRs (mmHg)
-0.12 (NS)
0.29 (NS)
0.12 (NS)
Diastolic blood pressure RRd (mmHg)
-0.15 (NS)
-0.09 (NS)
-0.06 (NS)
ACE (mU/ml)
ALDO/ARO index
**
-
-
-
-
-
R - correlation coefficients significant at: *p<0.05; **p<0.01; NS – No significant
Abbreviations: see Table 3.
Effect of AAS on the activity of RAAS
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Biol.Sport 22(2), 2005
Discussion
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Recent clinical and experimental studies proved the involvement of increased
activity of RAAS in pathogenesis of serious cardiovascular disturbances by
stimulation of heart muscle fibrosis (deposition of collagen type I and II) [25],
handicap diastolic and systolic heart function, left ventricle hypertrophy and blood
vessels fibrosis leading to cardiovascular inefficiency and sudden cardiac death
[5,6,7,27,30,36]. There was also reported that aldosterone can influence cardiac
arrhythmia and disturb coagulation properties of blood [7,8,25,35,42].
Aldosterone acts directly on the cardiovascular system influences without
elevation of blood pressure [6,27,31,36]. That is probably why, the increased
aldosterone level is regarded as an independent factor of the enlarged risk in
cardiovascular diseases [27].
Increased level of tissue aldosterone stimulates expression of converting mRNA
enzyme (ACE) causing an elevated synthesis of angiotensin II [36]. This mechanism
seems be confirmed by the results of the present work showing a significant
relationship between aldosterone level in blood plasma and ACE activity in body
builders.
A positive feed-back mechanism based on angiotensin II and aldosterone can be
involved in development of some cardiovascular diseases [36]. The angiotensin II,
through activation of AT1 receptors, enlarges aldosterone synthesis which trigger
tissue activity of ACE leading to further increase of the angiotensin II synthesis.
Aldosterone also increases sensitivity of AT1 receptors enhancing effects of
angiotensin II. Aldosterone increases the gene expression and modifies blood
vessels endothelium what elicit spastic action of coronary vessels, ischaemic state
and possible cardiac infractions [7,8,27,30,36]. Casuistic cases concerning abuse of
AAS and described in bibliography indicate some role of the above mentioned
mechanism in development of cardiovascular diseases [6,19,22,36].
In the study of Cubero et al. [4] aldosterone level measured in the group of 40
cyclists was similar to that observed in our cyclists. Similarly, in both discussed
works no relationship was found between aldosterone level in blood plasma and
heart dimension. These data suggest that aldosterone level has not significant
influence on physiological hypertrophy of heart muscle (athlete’s heart) in cyclist
not using AAS.
However, the significant relationship between aldosterone concentration in blood
plasma and the left ventricle mass of heart in body builders using large doses of
AAS would indicate that the level of activation of rennin-angiotensin-aldosterone
system could play an important role in pathogenesis of cardiovascular diseases. This
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hypothesis can be supported by a histopathological examination of a heart muscle
with hypertrophy (530 g) of a 21 years old weight lifter who died suddenly [2]. He
was taking the AAS (testosterone and nandrolone) during last few months before his
death. The examination showed advanced interstitial fibrosis of both ventricles,
atriums walls and coronary vessels. Similar changes were observed under
aldosterone excess in experiments performed on animals [2].
Nieminen et al. [22] described some pathological changes of the cardiovascular
system in 4 young weight lifters using large doses of anabolic steroids and
practising an intensive force training. The all 4 sportsmen had the heart muscle
hypertrophy, 2 of them showed cardiac insufficiency and in 1 subjects massive
thrombosis changes in both heart ventricles were found. Similar cardiovascular
changes in 2 body builders were reported by McCarthy et al. [17].
Pathogenesis of overgrowth of skeletal muscles and heart muscle hypertrophy in
subjects taking large doses of AAS is a complex process. It consist of many factors
including the insulin-like growth factor 1 (ILGF1) and tissue growth factor 1
(TGFβ1) [16,29,36]. However, participation of angiotensin II and aldosterone in this
process is essential [9].
Assuming the border values of the left ventricle mass (transferred into height
cm) over 1.7 g/cm [35], the heart mass index (left ventricle mass/body scope area –
MIM g/m2) over 143 g/m2 [14] and diastolic dimension of the left ventricle posterior
wall (PWd) (cm) between 1.2 and 1.3 cm [35] it was found that 4 body builders, 2
rowers and 9 cyclists exceeded those limits.
The highest values of the above indices were recorded in one body builder,
examined in 4th week of the cycle of AAS intake: MLK = 452 g; MLK/cm =2.58 g;
MIM = 196 g/m2; PWd = 1.4 cm. The echocardiography measurement repeated after
2 months of brake in AAS intake revealed the above indices diminished for about
16%, despite of the constant presence of AAS metabolites in urine samples.
The cardiological evaluation of both groups of body builders using the AAS and
former users showed normal haemodynamic efficiency of the circulatory system,
without pathological changes.
Conclusions
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 This study demonstrated a significant correlation between aldosterone level in
the blood plasma and mass of the left ventricle of heart, other echocardiography
parameters, body mass index (BMI) and ACE activity in the blood serum of body
builders. Rowers and cyclists showed a relationship between aldosterone level in
blood plasma and rennin plasma activity (ARO).
Effect of AAS on the activity of RAAS
203
Biol.Sport 22(2), 2005
 Obtained results suggest that the left ventricle hypertrophy and body mass
increase in men taking large doses of AAS may be an effect of strong activation of
tissue rennin-angiotensin-aldosterone system, what in connection with other
pathogenic factors (inflammatory states, toxic substances, injuries or strong stress)
may play an important role in pathogenesis of cardiovascular diseases.
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Accepted for publication 2.02.2005